期刊
CELL ADHESION & MIGRATION
卷 3, 期 1, 页码 94-98出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cam.3.1.7516
关键词
ischemia; intracellular Ca2+ dysregulation; changes of mitochondrial Ca2+; cytochrome c; apoptosis
类别
资金
- National Institutes of Health [R01NS-38118]
- Tsinghua-Yue-Yuen Medical Sciences Fund
- China Scholarship Council
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038118] Funding Source: NIH RePORTER
Ischemia-induced ionic imbalance leads to the activation of numerous events including mitochondrial dysfunction and eventual cell death. Dysregulation of mitochondrial Ca2+ (Ca-m(2+)) plays a critical role in cell damage under pathological conditions including traumatic brain injury and stroke. High Ca-m(2+) levels can induce the persistent opening of the mitochondrial permeability transition pore and trigger mitochondrial membrane depolarization, Ca2+ release, cessation of oxidative phosphorylation, matrix swelling and eventually outer membrane rupture with release of cytochrome c and other apoptogenic proteins. Thus, the dysregulation of mitochondrial Ca2+ homeostasis is now recognized to play a crucial role in triggering mitochondrial dysfunction and subsequent apoptosis. Recent studies show that some secondary active transport proteins, such as Na+-dependent chloride transporter and Na+/Ca2+ exchanger, contribute to ischemia-induced dissipation of ion homeostasis including Ca-m(2+).
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